Vulva dermatoses Flashcards
Blood supply to the female external genitalia
comes from the internal and external pudendal arteries
- Drains through corresponding veins
The external pudendal artery (branch of the femoral) has superficial and deep branches
Anterior division of the internal iliac artery –> internal pudendal artery
Within the pudendal canal
- Inferior rectal artery
- Perineal artery
Within the urogenital triangle
- The artery of the vestibule
- The deep artery of the clitoris
- The dorsal artery of the clitoris
Lymphatic drainage of the vulva
Via the inguinal glands
Perineum and vulva have bilateral lymph drainage
- 1 side can drain to the unilateral and contralateral LN
Nerve innervation to the vulva
Pudendal nerve (S2-4)
- Leaves the pelvis through the greater sciatic foramen and crosses the external surface of the ischial spines and re-enters the pelvis via the lesser sciatic notch, then splits into three
- Inferior rectal (haemorrhoidal) nerve
- Perineal nerve which branches into the posterior labial nerve
- Dorsal nerve of the clitoris
Branches of the ilioinguinal nerve (L1)
Genital branch of the genitofemoral nerve (L1-2)
The perineal branch of the femoral cutaneous nerve of the thigh (L2-4)
Development of the vulva - physiology
Birth to puberty:
- Absence of glycogen –> lack of lactobacilli –> neutral / alkalinity –> increased chance of vulvovaginitis, UTI
Oestrogen –> thickening of vaginal epithelium + appearance of intracellular glycogen –> pH falls to 4-5
If pregnancy occurs, vulva can become congested with varicosities from increased progesterone and gravid uterus
Menopause - Significant fall in oestrogen, progesterone
- Vagina becomes narrower, less rugose, drier
- Amount of cellular glycogen reduces, epithelium becomes thinner
- Vaginal pH becomes alkaline
LICHEN SCLEROSUS - aetiology
Auto-antibodies for extracellular matrix protein 1
Increased associated with other autoimmune diseases among patients (30% have autoimmune condition, 30% have family history)
- Thyroid disorders, alopecia areata, pernicious anaemia, T1DM, vitiligo - TEST TFTS / THYROID ABS
Higher incidence of disease in first degree relatives
- 10% FHx
LICHEN SCLEROSUS
- histology
Epidermal thinning (atrophic)
Hyperkeratosis
Wide band of collagen below the dermoepidermal junction
Lymphocytic infiltrate beneath this area
LICHEN SCLEROSUS
- clinical features
Two peak ages of presentation:
- Prepubescent girls (~5% of all cases)
- Post-menopausal women
Signs:
- Pale, white atrophic areas affecting the vulva
- Purpura (ecchymosis)
- Fissuring
- Erosions (but blistering is rare)
- Hyperkeratosis
- Localised or ‘figure of eight’ distribution
- Loss of architecture - loss of labia minora and/or midline fusion, burying of clitoral hood
- Extra genital lichen sclerosus in 1 in 10 (usually eyelids or back)
Does not involve the mucosa / vagina
LICHEN SCLEROSUS - treatment
No definitive treatment / cure - chronic Aim: - Relieve symptoms - Normalise appearance (prevent further changes) - Prevent scarring
Clobetasol proprionate 0.05%
- Daily for 1/12, alternate days for 1/12, twice weekly for 1/12, then review at 3/12
- Should have maintenance indefinitely
Good skin care
Emollients
Patient education is key
Follow up
- <5% risk of SCC
- once asymptomatic, yearly review
Lichen planus
- aetiology
Autoimmune inflammatory condition
Disorder of altered T-cell mediated immunity to exogenous antigens targeting the basal keratinocytes of the epidermis, genetic factors
Lichen planus
- clinical features
Usually post-menopausal (40-60y)
Typically presents with pain rather than pruritis
- Also vaginal discharge, sorenesss, burning, bleeding with sex
Erosion of mucosal surface of introitus, extending into vagina and involving cervix
Red, erythematous
- Lacy white lines (Wickham’s striae) in surrounding skin / on top
Vaginal lesions can lead to scarring and complete stenosis
Oral and genital lesions together in 70%
Three variants
- erosive - most common
- classical
- hypertrophic
Lichen planus
- histology
Lymphocytic infiltrate in the upper dermis directed against the basement membrane zone
Irregular saw-toothed acanthosis
lack of basement membrane thickening or epidermal atrophy favour lichen planus over lichen sclerosus
Lichen planus
- treatment
Limited evidence - treatment resistant Topical steroids (clobetasol propionate) Topical tacrolimus Oral steroids, retinoids, immune suppression refer specialist
Lifetime risk of invasive vulval cancer in the order of 2-4%
Contact dermatitis - irritant
Pathogenesis
Due to skin injury by prolonged pressure and irritation, chemical or physical agents –> inflammation
Reduces the integrity of the epidermis increasing the irritancy of irritants
Immediate, non-immunological, local inflammatory reaction
Can get secondary infection
More common (80%) than allergic contact dermatitis
Contact dermatitis - allergic
Caused by immune response following skin contact with an allergenic substance
Classical delayed-type hypersensitivity reaction (type IV, T cell mediated)
Identify allergen by patch teaching
Clinical features of contact dermatitis
Well demarcated margins in area of contact
Erythema, erosions, ulcers, tissue destruction
Increases with multiple exposure
Irritant - Rapid onset of Sx (mins to hrs)
Allergic - Delayed onset (1-2 days)
- may occur at distant site
Advice for contact irritant dermatitis
Avoid soaps, bubble baths, deodorants, feminine sprays, vaginal wipes
- Use non-perfumed emollient soap
Clean the vulval area with water only, showers > baths
If PU –> worse symptoms, wash urine away using warm water
Clean once a day only - Avoid scrubbing
Avoid creams that have not be prescribed
Avoid anti-septics in the bath
Wear loose-fitting cotton underwear
Use lubricants during sex
Use tampons over pads
Only apply creams and ointments where needed
- Ointments less likely to irritate and have fewer potential sensitisers
No G strings, jeans, lyra gym pants
No vaginal douching
Histology of contact dermatitis
Variable features - key feature = spongiosis, irregular hyperkeratosis of epidermis
Allergic - more eosinophils
Contact - less eosinophils
Treatment for contact dermatitis
If obese, weight reduction may help
Emollients - e.g. aqueous cream
Manage urinary incontinence
Topical corticosteroids with anti-bacterial / fungal
VULVAL ECZEMA = ATOPIC DERMATITIS
Uncommon, even with widespread eczema
chronic inflammatory dermatosis characterised by relapsing episodes of flares of intensely pruritic, inflammatory skin lesions
Occasionally skin scaling and fissuring
Usually have eczema elsewhere
Spongiosis = intercellular oedema - characteristic of eczematous dermatitis
LICHEN SIMPLEX CHRONICUS
- aetiology
Acquired severely itching chronic dermatosis characterised by a non-scarring process of epidermal thickening due to repeated scratching
Primary / idiopathic - on background of normal skin
Secondary - may be an underlying cause (e.g. lichen planus or lichen sclerosus)
LICHEN SIMPLEX CHRONICUS
- clinical features
Long Hx of pruritis that hasn’t responded to any topical agent
May be worse at times of stress, at night
Asymmetry of the vulval lichenification with the clinically obvious side being the same side as the dominant hand
Mostly affects hair-bearing skin of labia majora
- Skin thickening, erythematous lichenified plaques, leathery feeling skin
- Skin excoriation, erosions, ulcers
LICHEN SIMPLEX CHRONICUS
- histology
Hyperplasia of squamous epithelium, thickened epidermis, and hyperkeratosis – not atrophy / thinning as in lichen sclerosus
Spongiosis
Lichen simplex chronics
- management
Treat underlying dermatoses / systemic disease
Remove triggers / exacerbating factors
Break the ‘itch-scratch cycle’
Topical corticosteroids (if lichenified areas)
Antihistamines at night to help sleep
Emollients
Repair barrier function of skin
Define Hyperalgesia
exaggerated response to noxious substances through a general increase in the responsiveness of tissues
Allodynia
production of pain by stimuli that does not usually cause pain by a reduction in the sensory threshold of the local neuronal pathways
Vulvodynia - aetiology
and definition
Lifetime: 10-15%
Vulvodynia - vulvar pain of at least 3 months without clear identifiable cause, which may have potential associated factors
- diagnosis of exclusion
Chronic pain pathophys
2 neurophysiological mechanisms implicated
Nociceptive
- Injury to a pain sensitive structure
- Somatic, visceral
Non-nociceptive
- Neuropathic
○ Pain as a result of changes in the nerve itself
○ Result of an insult to the CNS or PNS
○ Typical characteristics - burning pain, paraesthesia, lancinating pain
- Psychogenic
Key history for vulvodynia
Unprovoked
- Continuous sensation
- Spontaneous pain
- Itching not usually a problem
Provoked
- Pain with light touch
- Usually no symptoms at other times
- May be multifactorial - Hx of vulvovaginal candidiasis is the most common feature
Localised, generalised
Aggravating and relieving factors
Psychosexual Hx
Co-morbidities and other pain syndromes (e.g. painful bladder syndrome, fibromyalgia, IBS, temporomandibular disorder)
Treatment principles of vulvodynia
MDT - gynaecologist, physiotherapy, psychologist, pain specialist
The aim of therapy is to optimise pain control, enhance psychological and physical wellbeing and improve quality of life
The end points in the treatment include reducing the triggers of irritation, blocking peripheral nociceptors, central inhibition, tackling pelvic floor dysfunction and addressing psychosexual dysfunction
The “4 Ps”
- Patient education and reassurance
- Pain modification
- Physical therapy
- Psychological and psychosexual therapy
Treatment of provoked vulvodynia
Avoid irritants Emollient soap substitute Topical LA (2 or 5%) - use with caution Pelvic floor muscle biofeedback Vaginal TENS Vaginal dilators Vestibulectomy - Surgical removal of hyperaesthetic skin - If responded to topical lidocaine prior to sex, more likely to have a better outcome - Complete response rate 59%
Genital warts - aetiology
90% caused by HPV 6 or 11
Transmission
- Sexual contact - Condoms reduce but do not eliminate risk
- Perinatal
Average incubation period 3 months
90% reduction in cases (15-20y) since Gardasil introduced
Treatment options for genital warts
Is largely cosmetic
30% have spontaneous clearance over a 6 month period
No evidence Rx reduces risk of transmission
Imiquimod cream 5%
- Topical, patient applied
- Can weaken latex condoms, local skin irritation
Podophyllotoxin solution
- Avoid in pregnancy
- Patient applied
Cryotherapy - Freezing therapy
- can do in pregnancy
Diathermy, laser, excision
- Single treatment
- Can distort anatomy
- may need GA
Genital warts in pregnancy
Common for warts to occur / recur during pregnancy
More likely to be symptomatic
- Anogenital warts can be extensive and rapidly enlarging
- Likely consequence of altered immunity and increased blood supply
Vertical transmission of HPV occurs in up to 1 in 80
- Can cause genital and laryngeal warts in infants
CS can be consider if large warts that may obstruct labour or that cause extensive cervical disease
Otherwise not indicated
Expectant vs. active treatment for warts
The treatment of genital warts is largely cosmetic
They can spontaneously regress in 30% people over the course of 6 months
No evidence that treating warts lowers risk of passing on HPV
Reassure low oncogenic potential
Active treatment can be indicated:
- If the patient requests it
- If they are symptomatic or causing irritation
Recurrence of 30% regardless of treatment
Psychological impact
